| Objective:Ghrelin, an endogenous ligand for the growth hormone (GH) secretagogue receptor, was originally purified from the rat stomach. We have previously reported that central administration of ghrelin increases food intake and body weight. To investigate the role of ghrelin in the hyperphagia response to uncontrolled diabetes.Method:Intraperitoneal injection of STZ to establish Type I diabetes rat model. Observe the chaμge of blood glucose levels and food intake and body weight of diabetic rats, and the influence and the possible mechanismof insulin therapy.Results:The blood glucose levels of diabetes rat have A significant rise (t=3.71~6.38, P<0.01), Food intake increased significantly (t=2.31~2.85, P<0.05), Significant reduction in weight (t=2.34~2.70, P<0.05); After insulin therapy, Blood glucose levels decreased significantly in rats (t=2.27~2.85, P<0.05), Food intake was significantly reduced (t=2.52~2.77, P<0.05), Weight increased significantly (t=2.44~2.65, P<0.05).After14days of Diabetic rats, Plasma insulin and leptin levels were significantly reduced (t=3.08, t=7.86, P<0.01), After insulin therapy,Plasma leptin levels increased significantly (t=13.03, P<0.01).Diabetic rat hypothalamic NPY mRNA expression and plasma ghrelin levels were significantly increased (t=48.77, t=6.39, P<0.01), both were close to normal level after insulin treatment (t=0.49, t=0.43, P>0.05). Intravenous Ghrelin receptor antagonist [D-Lys-3]-GHRP6can significantly reduce food intake of diabetic rats (t=6.3, P<0.05).Conclusion:STZ induced diabetic rats plasma ghrelin levels increase, lower leptin levels, and increased expression of ghrelin, all can lead to the formation of excessive feediμg of diabetes. |